Metabolic disorders

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Chapter 27 Metabolic disorders

Diane King, Derek Louey

ELECTROLYTE EMERGENCIES

Theory

• Serum electrolyte concentrations are usually tightly controlled unless excessive gains or losses overwhelm homeostatic balance.
• Electrolyte balance requires normal hormonal control of intact kidney function. Primary renal dysfunction or the effects of drugs or endocrine disease can result in abnormalities.
• Water and electrolytes can be mobilised between plasma and other body compartments. This may occur under hormonal control.
• Serum electrolyte concentrations do not necessarily correlate with total body stores.

Causes/assessment

• Electrolyte losses: renal (drug effects or endocrinopathy), GIT (vomiting, diarrhoea, surgical drains), skin (sweating, burns)
• Electrolyte gains: ↓ renal elimination (renal failure, drug effects, endocrinopathy), GIT (diet, drugs), iatrogenic (intravenous therapy (IVT), total parenteral nutrition (TPN))
• Body compartment shifts: intracellular (e.g. potassium), bone (e.g. calcium, phosphate, magnesium)

Clinical effects

• Electrolytes have a role in establishing the membrane potential, receptor signalling and enzyme function.
• Depending on the electrolyte abnormality the central nervous system (CNS), cardiovascular system (CVS) and/or neuromuscular system can be affected.
• Clinical effect can vary from mild and non-specific to severe and life-threatening.
• Clinical impact is proportional to the severity and acuity of the derangement.
• If results are inconsistent with clinical information, repeat the test.

Management

Treat the patient, not just the abnormality.

• Mild cases—review and address causes, monitor abnormality.
• Moderate cases—as above plus begin treatment.
• Severe, life-threatening or resistant cases, e.g. neurological (seizures, coma), CVS (hypotension, abnormal ECG), respiratory muscle failure (hypoventilation, tetany)—get input from the intensive care unit (ICU).

Find and treat the cause, not just the abnormality. Often there is more than one mechanism operating, e.g. poor oral intake plus diuretic.

(See Table 27.3 for a list of electrolyte abnormalities, clinical indications and treatment.)

Table 27.3 Electrolyte emergencies (ICU involvement required)

image

ACID–BASE DISTURBANCES

Pearls/pitfalls

• An acute derangement in acid–base balance invariably signifies a significant disease process (most patients need admission or at least extended observation).
• An abnormal or recent change in venous bicarbonate may be the first clue to an acid–base disturbance.
• Arterial blood gas (ABG) determination is essential to fully categorise the disturbance, e.g. acidosis/alkalosis, respiratory/metabolic or mixed. Don’t just look at pH.
• Clinical information and other lab tests will help determine the cause.
• Treatment should primarily be directed at the cause of the disturbance and not by directly manipulating pH, e.g. sodium bicarbonate is indicated in only a limited number of causes of metabolic acidosis.

Normal values

• pH: 7.35–7.45
• pCO2: 35–45 mmHg (‘respiratory acid’)
• pO2: 100 mmHg
• [HCO3–]: 24 mmol/L (‘metabolic base’)

Determining the acid–base abnormality

1. Check pH: < 7.4 (acidaemic) or > 7.4 (alkalaemic)

• If acidaemic: is [HCO3–] < 24 (metabolic acidosis) or pCO2 > 40 (respiratory acidosis) or both?
• If alkalaemic: is [HCO3–] > 24 (metabolic alkalosis) or pCO2 < 40 (respiratory alkalosis) or both?

2. Is the respiratory compensation for a metabolic abnormality appropriate? (See ‘Metabolic equations’ in the ‘Quick reference’ section at the beginning of this book.)

• If pCO2 lower than expected: = concurrent respiratory alkalosis
• If pCO2 higher than expected: = concurrent respiratory acidosis

3. Is the metabolic compensation for a respiratory abnormality acute/incomplete or chronic/complete? (See ‘Metabolic equations’ in the ‘Quick reference’ section.)

• If [HCO3–] lower than expected: = concurrent metabolic acidosis
• If [HCO3–] higher than expected: = concurrent respiratory acidosis

Anion gap

• Anion gap approximates the unmeasured anions (usually [protein–], [SO42–], [PO43–]).
• Can be estimated as:

image

• Anion gap is diagnostically useful in metabolic acidosis (see below).
• A wide anion gap in the setting of metabolic alkalosis is suggestive of concurrent metabolic acidosis.

Metabolic acidosis

(Mild: [HCO3–] < 18 mmol/L; moderate: < 15 mmol/L; severe: < 12 mmol/L)

This is the commonest metabolic abnormality seen in the emergency department. Frequently under-recognised and under-treated (low venous HCO3– on serum electrolytes is the first clue). pH may be (temporarily) near normal if well compensated.

• Important causes of wide anion gap metabolic acidosis: poor tissue perfusion, hypovolaemia and/or sepsis (most common), diabetic ketoacidosis (DKA), renal failure, drug poisoning.
• Rare but important causes: thiamine deficiency, metformin.
• Less common causes: bicarbonate loss from GUS or GIT/‘normal anion gap metabolic acidosis’ e.g. renal tubular acidosis, surgical fistula/stomal/drain losses, Addison’s disease.
• Rapidly assess the following—circulatory status (HR, BP, urine output), infection (fever), hyperglycaemia (bedside blood sugar level (BSL), urinary ketones).
• Important lab tests—electrolytes, anion gap, renal function, serum osmolarity, serum ketones, BSL, WCC.

Management

1. Treat cause:

• hypovolaemia—fluid challenge until vital signs and urine output restored
• sepsis—fluid challenge, early administration of antibiotics
• DKA—see Chapter 26, ‘Endocrine emergencies’
• renal failure—see below
• poisoning—obtain toxicology advice
• normal anion gap acidosis—bicarbonate infusion.

2. Potassium deficit may be unmasked as the metabolic acidosis resolves. Begin replacement if already hypokalaemic or when adequate urine output established (see ‘Management’ under ‘Hyperkalaemia’).

Metabolic alkalosis

(Mild: [HCO3–] > 25 mmol/L; moderate: > 30 mmol/L; severe: > 35 mmol/L)

• Common causes in emergency department include: diuretic use, gastric losses (e.g. pyloric stenosis, bulimia nervosa).
• Less common causes: excessive corticosteroids (Cushing’s syndrome, hyperaldosteronism).
• Perpetuating factors: dehydration, hypokalaemia.

Management

1. Most are ‘saline (chloride) responsive’ (urine [Cl–] < 25 mmol/L)—correct dehydration with normal saline (contraindicated in oedematous states).
2. Potassium depletion needs to be corrected (see ‘Hypokalaemia’).
3. Stop offending medications.
4. Treat cause.
5. If ‘saline unresponsive’ [urine [Cl–] > 40 mmol/L], may need HCL via central venous catheter (CVC) (manage in ICU).

Respiratory acidosis

(Mild: pCO2 > 45 mmHg; moderate: > 55 mmHg; severe > 65 mmHg)

• Any cause of respiratory depression or inadequate alveolar ventilation.
• Common emergency department causes include: acute cardiorespiratory illness (asthma/COAD, pulmonary oedema, pneumonia), CNS insults (opiates, benzodiazepines, acute space-occupying lesion), trauma (head injury, flail chest, haemo/pneumothorax).

Management

1. Treat cause.
2. Mechanical ventilation (especially if drowsy/somnolent, severe head injury).
3. Common mistake—decreasing fraction of inspired oxygen (FiO2) in an already hypoxic patient (aim for SpO2 90–93% if CO2 retention is of concern).

Respiratory alkalosis

Unusual but important causes: sepsis, pulmonary embolism, salicylate poisoning (do not assume anxiety)

HYPONATRAEMIA

(Mild < 130 mmol/L; severe < 110 mmol/L)

• Mild/moderate or chronic cases may be asymptomatic or have non-specific clinical features (correct abnormality slowly or risk of central pontine myelinolysis).
• Life-threatening: cerebral oedema, seizure, coma (requires immediate treatment with hypertonic saline).
• Common causes:

• water excess—secretion of inappropriate antidiuretic hormone (SIADH), excessive water intake, too much 5% dextrose
• sodium loss—diuretics, GI losses, excessive sweating
• ‘oedematous states’—severe heart failure, liver cirrhosis.

• Review drug history.

Table 27.1 Assessment of hyponatraemia

image

Classic pictures

• Low Na+, K+, CL–—‘drip arm’
• Low Na+, high serum osmolarity—DKA, hyperosmolar nonketosis (HONK), mannitol
• Low Na+, high UNa/Uosm—SIADH, Addison’s disease
• Low Na+, normal serum osmolarity—‘pseudohyponatraemia’

Management

1. If seizures or coma, GET HELP (see Table 27.3, ‘Electrolyte emergencies’).
2. If in shock or oliguric—bolus IV normal saline.
3. If circulatory parameters normal and good urine output—fluid restriction 1000 mL/day (aim to increase Na+ by 5–10 mmol/L/day).
4. Over-rapid correction may lead to central pontine myelinolysis and quadraparesis.
5. Oral salt supplementation is generally not required.

HYPERNATRAEMIA

(Mild > 145 mmol/L; symptomatic > 155 mmol/L)

• Mild or chronic cases may be asymptomatic or have non-specific clinical features.
• Altered mental state occurs in severe cases.
• Slow correction is the general rule (otherwise risk of cerebral oedema).
• Common causes:

• inadequate water intake—institutionalised patients, impaired conscious state
• excess water loss—GI losses, diabetes insipidus (DI) (rare but important).

Assessment

• Plasma osmolarity, urine sodium, urine osmolarity (low in DI).
• Review drug history.

Management

1. If in shock or oliguric—bolus IV saline.
2. Slow correction with half normal saline or 5% dextrose over 48–72 hours; total water deficit usually around 5–10% of body weight.
3. Repeat electrolytes at least daily; aim to reduce by 5–10 mmol/L/day (over-rapid correction may lead to cerebral oedema).
4. If DI: vasopressin/desmopressin (obtain assistance).

OSMOLARITY, OSMOLAR GAP

• Osmolarity equals the amount of osmotically active substances (normal ∼ 285 mosm/L).
• Plasma osmolarity (Posm) can be estimated from the electrolyte panel:

image

• Posm can also be accurately measured directly in the lab by freezing point depression.
• Osmolarity is usually proportional to [Na+].
• Osmolar gap = measured osmolarity – estimated osmolarity.
• In the setting of acute poisoning and the absence of lactic or ketoacidosis, a raised osmolar gap suggests ingestion of osmolar acting substances such as ethanol, methanol or ethylene glycol.

URINE OSMOLARITY AND OTHER URINE ELECTROLYTES

• In homeostasis, urine electrolyte concentration is altered constantly to maintain serum concentration in constant range.
• With normal hormonal and renal control, changes in urine composition should match changes in serum concentration. i.e. ↑ serum [Na+] should be matched with ↑ urine [Na+].
• Loss of this relationship suggests renal or endocrine dysfunction is contributing to the electrolyte abnormality.
• Urine osmolarity (Uosm) normally is inversely proportional to the state of hydration (range: 50–1200 mosm/L).
• Urine and plasma osmolarity that move towards opposite extremes suggest endocrine or renal dysfunction, e.g. high (Posm) and low (Uosm) = SIADH.

HYPOKALAEMIA

(Mild < 3.5 mmol/L; severe < 2.4 mmol/L)

• Can cause muscle weakness (e.g. hypokalaemic period paralysis).
• Most dangerous complication is ventricular arrhythmia.
• ECG—flat T waves, U waves.
• Common causes: potassium losses—GI losses, laxatives, diuretics, sweating.

Management

• Life-threatening (acute arrhythmia)—GET HELP (see Table 27.3, ‘Electrolyte emergencies’), ultra-rapid IV potassium should be performed in ICU.
• Severe or nil by mouth (< 2.5 mmol/L)—10–20 mmol/L normal saline/h (> 40–60 mmol/L concentration needs to be given by central line).
• Mild/moderate (2.5–3.5 mmol/L)—slow K 600–1200 mg/day or Chlorvescent 2–3 tablets/day.

Successful treatment is dependent on addressing concurrent hypomagnesaemia (see ‘Hypomagnesaemia’).

HYPERKALAEMIA

(Mild > 5 mmol/L; severe > 7.5 mmol/L)

• Most dangerous complication is ventricular arrhythmia (do immediate ECG).
• ECG—peaked T wave > PR prolongation > QRS prolongation > sine wave.
• Common causes in emergency department patients:

• inadequate potassium excretion—renal failure, K-sparing diuretics, hyperaldosteronism
• cellular injury—crush injury, rhabdomyolysis, haemolysis
• transcellular shifts—metabolic acidosis.

Management

• Life-threatening (QRS widening, arrhythmia): GET HELP (see Table 27.3, ‘Electrolyte emergencies’), NaHCO3 1 mmol/kg over 30 minutes if concurrent metabolic acidosis, may need dialysis.
• Moderate (> 6.5 mmol/L): IV 50% dextrose + IV 5–10 units Actrapid + 10 mg salbutamol nebuliser + above.
• Mild (> 5 mmol/L): review cause ± rehydrate, resonium 30 g PO/PR.

Note: Most treatments only result in temporary transcellular shifts of potassium. Kaliuresis, dialysis or resonium will result in true elimination of potassium.

HYPOCALCAEMIA

(Symptomatic: total Ca2+ < 1.8 mmol/L, ion Ca2+ < 0.7 mmol/L)

• Can present with tetany, paraesthesia or bradyarrhythmia.
• Possible causes: acute pancreatitis, acute renal failure, tumour lysis syndrome, post-thyroid/parathyroidectomy.

Management

• If breathing difficulties or bradyarrhythymias: GET HELP (see Table 27.3 ‘Electrolyte emergencies’).
• Moderate/chronic: 60–120 mL 10% calcium gluconate in 1 L 5% dextrose over 24 hours.
• Mild, chronic: caltrate, calcitriol.

HYPERCALCAEMIA

(See also Chapter 42, ‘The immunosuppressed patient’, ‘Hypercalcaemia’).

(Mild > 2.5 mmol/L; severe > 3.5 mmol/L)

• Can present with changes in mental state/confusion (always consider this in cancer patients).
• Common causes: malignancy/bone metastases, sarcoidosis, ↑ parathyroid hormone (PTH)

Management

Note: All therapies take time to work.

1. If comatose: GET HELP (see Table 27.3, ‘Electrolyte emergencies’).
2. Correct dehydration until adequate urine output.
3. Commence saline calciuresis: IV saline 1000 mL/6 h ± 20 mg frusemide/2 h.
4. Other treatments: IV phosphate, bisphosphonates, calcitonin, gallium arsenide.

HYPOPHOSPHATAEMIA

(Moderate < 0.8 mmol/L; severe: < 0.4 mmol/L)

• Can present with paraesthesia, mental state changes or arrhythmias.
• Common causes: following DKA treatment, re-feeding malnourished patient, chronic alcoholism, ↑PTH.

Management

• If arrhythmia: GET HELP (see Table 27.3, ‘Electrolyte emergencies’).
• Moderate: IV KH2PO4/K2HPO4 40–80 mmol/L in 1 L normal saline per 24 h.
• Mild: resume normal diet.

HYPERPHOSPHATAEMIA

• Can present with seizure or arrhythmia.
• Possible causes: acute tissue breakdown (rhabdomyolysis, haemolysis, tumour lysis), phosphate enemas.

Management

Note: All therapies take time to work.

• If seizures, arrhythmia: GET HELP.
• Moderate/severe: commence urgent saline rehydration. Consider dialysis (especially with concurrent hypocalcaemia).
• Mild: maintain hydration, address cause.

HYPOMAGNESAEMIA

(Symptomatic < 0.5 mmol/L)

• Can present with tetany, paraesthesia or bradyarrhythmia.
• Common causes: diuretics, chronic alcoholism, poor nutrition

Management

• If major symptoms: GET HELP (see Table 27.3, ‘Electrolyte emergencies’).
• Moderate: IV MgSO4 20–60 mmol in 1 L normal saline over 24 h.
• Mild: magnesium chloride 25–50 mmol over 24 h.

HYPERMAGNESAEMIA

(Mild > 2 mmol/L; moderate > 3.5 mmol/L; severe > 5 mmol/L)

• May have hypotonia/reflexia, mental state changes.
• Major complications: respiratory muscle weakness, arrhythmia, hypotension.
• Common causes: acute renal failure, iatrogenic (e.g. treatment of eclampsia)

Management

Note: All therapies take time to work.

• If cardiorespiratory compromise: GET HELP (see Table 27.3, ‘Electrolyte emergencies’).
• Rehydrate ± dialysis.

Table 27.2 Approximate correction factors for electrolyte abnormalities

Situation Correction∗
Hyperglycaemia True [Na+] = measured [Na+] + ([Gluc] ÷ 4)
Metabolic acidosis Reduce measured [K+] by 0.5 for every ↓ pH 0.1
Metabolic alkalosis Increase measured [K+] by 0.5 for every ↑ pH 0.1
Hypoalbuminaemia Add 0.1 total [Ca2+] for every 4 g/dL decrease in albumin

∗ All measurements in mmol/L. Corrections are rough guides.

ACUTE RENAL FAILURE

ANY of the following:

• ANY rise in serum creatinine (normal < 120 μmol/L)
• urine output < 30 mL/h

Life-threatening complications

• Severe hyperkalaemia (see ‘Hyperkalaemia’)
• Acute pulmonary oedema
• Uraemic encephalopathy

Early emergency department assessment and management

(‘Pre-renal, renal, post-renal’)

1. Assess for and treat hyperkalaemia (see ‘Hyperkalaemia’).
2. Restore renal perfusion—IV fluid bolus until urine output > 40 mL/h or fluid overload develops.
3. Treat sepsis or UTI—urine dipstick, urine culture, IV antibiotics.
4. Relieve obstruction—indwelling catheter (IDC) and measure hourly urine output ± urgent renal ultrasound to exclude ureteric obstruction ± urgent nephrostomy, beware of post-obstructive diuresis resulting in hypovolaemia, hypokalaemia.
5. Stop nephrotoxic drugs—e.g. NSAIDs, aminoglycosides, ACE-I, frusemide.

Pre-renal (dehydration/hypovolaemia) or established (acute tubular necrosis) renal failure?

• Typically, in pure dehydration, ↑ Plasma urea >> ↑creatinine rise.
• ‘Intra-renal’ causes—check urine sediment for casts, protein and cells.

(See Table 27.4, ‘Pre-renal vs renal failure’.)

Table 27.4 Pre-renal versus renal failure

Cause/mechanism Pre-renal failure Established renal failure (i.e. ATN)
Summary Maximal water and sodium retention and maximally concentrated urine to maintain circulatory volume (UNa ↓ but Uurea,, Uosm,,Ucreat ↑↑↑) Loss of concentrating power volume (UNa ↑ and Uurea, Uosm,,Ucreat ↔)
UNa (mmol/L) < 20 > 40
Uurea > 450 > 300
Uurea😛urea > 20:1 < 10:1
Uosm > Posm > 2:1 < 1:2
Ucreat😛creat 40:1 20:1

ATN, acute tubular necrosis/renal failure; Pcreat, plasma creatinine; Posm, plasma osmolarity; Purea, plasma urea; Ucreat, urinary creatinine; Uosm, urinary osmolarity; UNa, urinary sodium.

Indications for haemodialysis

(‘Too much acid, water, potassium or poison’)

• Severe metabolic acidosis
• Acute pulmonary oedema—fluid challenge does not re-establish urine output
• Hyperkalaemia not responding to medical treatment (see ‘Hyperkalaemia’)
• Acute nephrotoxic exposures, e.g. lithium, methanol, ethylene glycol

Controversies in electrolyte management

• Use of bicarbonate in severe wide anion gap metabolic acidosis pH < 6.8
• Cause of cerebral oedema in DKA—iatrogenic or idiopathic?
• 5% dextrose, half normal saline or normal saline for hypernatraemia
• Excessive IV fluid volume unmasking SIADH and hyponatraemia
• Cause of central pontine myelinolysis in hyponatraemia—iatrogenic or idiopathic?
• Use of diuretics to convert oliguric renal failure into non-oliguric renal failure
• At what creatinine level to commence dialysis?

Hyperlactataemia or ‘lactic acidosis’—clinical use, prognostication, disposition

[Normal value < 2 mmol/L (‘significant’ > 5 mmol/L)]

• The body does not produce ‘lactic acid’.
• Hyperlactataemia can occur with or without concurrent acidaemia.
• Causes of raised lactate levels (often several mechanisms coexist):

• increased glycolytic activity e.g. exercise, hyper-metabolic states, critically ill patients
• reduced metabolism, e.g. severe liver dysfunction
• poor tissue perfusion/oxygenation (type A lactic acidosis)—important cause
• abnormal mitochondrial function (type B lactic acidosis)—e.g. metformin, thiamine deficiency.

• Severity generally correlates to short- to mid-term morbidity and mortality (> 8–10 mmol/L predicts high mortality).
• Transiently high elevations can occur after prolonged exertion or seizures.
• Levels may be chronically elevated, e.g. chronic liver failure.
• Serial measurements (and response to treatment) have higher prognostic value than a single test.
• The interpretation (as in all investigations) needs to consider other clinical data, i.e. other evidence of hypoperfusion, the disease process, its acuity and how readily it responds to treatment (e.g. haemorrhagic shock versus severe sepsis/multi-organ failure versus end-stage chronic liver failure).
• Its main application in the acute setting is to support a clinical suspicion of poor tissue perfusion or inadequate response to fluid/inotropic support.
• A normal lactate should not override clinical judgement.

RECOMMENDED READING

Broder G., Weil M. Excess lactate: an index of reversibility of shock in human patients. Science. 1964;143:1457-1459.

Cooper SC, Nathan DM, Snyder PJ, eds. Endocrinology and diabetes [e-book]. Waltham, MA; UptoDate; 2008. Online. Available from: UptoDate. http://www.uptodate.com/home/index.html.

Stacpoole P., Wright E., Baumgauter T., et al. Natural history and course of acquired lactic acidosis in adults. Am J Med. 1994;97:47-54.

Walmsley R.N., White G.H.. A guide to diagnostic clinical chemistry, 3rd edn. Blackwell Scientific Publications, Melbourne, 1994.

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